S3584 Captopril-Associated Pancreatitis in a Patient With Scleroderma Renal Crisis: A Post-COVID Multisystem Complication

Introduction: Medications are the underlying etiology in less than 5% of pancreatitis cases, with ACE-inhibitors accounting for a small portion of those reported. Captopril is first-line treatment for scleroderma renal crisis (SRC) and is associated with proven mortality benefits. Herein, we present a case of a woman started on captopril for SRC who developed pancreatitis complicated by pseudocysts, requiring cystogastrostomy. Case Description/Methods: A 66-year-old woman presented with diffuse weakness, skin changes, and joint pain, 6 months after a coronavirus disease 2019 (COVID-19) infection. Labs at that time revealed microangiopathic hemolytic anemia and the presence of SCL-70 antibodies. She was initiated on captopril and mycophenolate for concerns of SRC. Several weeks after initiating therapy she developed postprandial epigastric pain. Her lipase was minimally elevated and a computed tomography scan showed peripancreatic edema. She had moderately delayed gastric emptying and retained gastric contents were seen on esophagogastroduodenoscopy. She continued to have persistent abdominal pain with repeat computed tomography scans showing the development of multiple large pseudocysts with 1 compressing on the stomach. Magnetic resonance cholangiopancreatography (MRCP) showed no biliary duct dilation. She underwent cystogastrostomy for symptomatic relief. The hospital course was complicated by cardiac tamponade, acute tubular necrosis requiring dialysis, and septic shock ultimately resulting in end of life. Discussion: Several case reports have indicated a possible link between COVID-19 infections and subsequent scleroderma development, with SRC representing a particularly severe complication. New onset hypertension, rapidly progressing kidney injury, microangiopathic hemolytic anemia, and thrombocytopenia are pathologic manifestations of the excessive renin-angiotensin aldosterone system (RAAS) activation characteristic of SRC. Captopril directly targets RAAS and is therefore the preferred therapeutic option. The exact mechanism of ACE-inhibitor induced pancreatitis is poorly understood. Current theories suggest pancreatic duct obstruction by local angioedema and direct acinar cell toxicity. In this case, the temporal relationship with captopril initiation and absence of alternative explanations support a drug-induced etiology. Although rare, ACE inhibitor associated pancreatitis has been reported in multiple case reports. This underscores the importance of maintaining a high index of clinical suspicion to facilitate early recognition, which is essential in preventing serious complications.